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PubMed1982

Changes in intrarenal uric acid handling during chronic spironolactone treatment in patients with essential hypertension.

Intrarenal handling of uric acid was studied in 12 patients with essential hypertension under spironolactone treatment (200 mg/day). The degree of volume depletion during treatment was assessed from the changes in body weight and plasma renin activity (PRA). The results are compared with those in patients treated with chlorthalidone (50 mg/day). During spironolactone treatment, the serum uric acid level remained constant despite a progressive volume depletion which after 3 months reached levels identical to those achieved in the chlorthalidone-treated patients, whose serum uric acid level showed the expected rise (21%). The uric acid excretion during spironolactone treatment was markedly diminished (-28%), and thus the 24-hour clearance of uric acid was correspondingly decreased (-22%). It is concluded that spironolactone affects uric acid metabolism in two ways: it causes a decrease in uric acid renal clearance (probably mediated by the induced volume depletion and PRA elevation, as with other saluretics) and, probably, inhibits endogenous uric acid production to approximately the same degree as the clearance is decreased, so that no change in the serum uric acid level occurs. The purpose of the study was to investigate the effect of spironolactone on uric acid handling by the kidney. We found a decrease in uric acid clearance and uric acid excretion. Serum uric acid concentration did not change.

Body Weight↗
PubMed1986

Uric acid protection of nucleobases from ozone-induced degradation.

Uric acid has been proposed to be an important antioxidant and free radical scavenger in humans. Of the purine and pyrimidine compounds examined in this study, uric acid showed the greatest susceptibility to ozone-induced degradation. The parent compounds, purine and pyrimidine, were more resistant to ozonation than were the nucleobases. When the degradation of OH-substituted purines was examined, it was found that the more OH groups on the purine ring, the more readily the purine was degraded. Urea and allantoin were identified as degradation products of uric acid. The relative rates of nucleobase degradation in the presence and absence of uric acid were compared. Uric acid protected thymine, guanine, and uracil from degradation by ozone. In this system uric acid was found to protect the nucleobases as effectively as reduced glutathione.

Antioxidants↗
PubMed1986

Serum uric acid, serum glucose and diabetes: relationships in a population study.

The relationships between serum uric acid, serum glucose and diabetes have been examined in a survey of 7735 middle-aged men drawn at random from general practices in 24 British towns. There was a positive relationship between serum glucose and serum uric acid concentrations up to about 8.0 mmol/l; at higher levels of glucose, serum uric acid decreased. Uric acid levels were significantly reduced in insulin-dependent diabetics and in those on oral hypoglycaemics and also in 'non-diabetics' with casual glucose levels greater than 10 mmol/l. Both uric acid and glucose concentrations were positively related to body mass index; only uric acid was positively related to alcohol intake. Men on antihypertensive treatment had raised levels of uric acid (significant) and glucose (non-significant). The positive relationship between serum uric acid and serum glucose could not be explained by associations with body mass index, alcohol intake, age, social class, gout or treatment for hypertension. It probably reflects the biochemical interaction between serum glucose and purine metabolism, with increased excretion of uric acid during hyperglycaemia and glycosuria.

Adult↗
PubMed2006

A novel electrochemical biosensor for the detection of uric acid and adenine.

A novel electrochemical biosensor for the detection of uric acid and adenine was prepared based on a gel containing multi-walled carbon nanotubes and room-temperature ionic liquid of 1-octyl-3-methylimidazolium hexafluorophosphate. The electrochemistry of uric acid and adenine was studied in this gel modified electrode. There was a significant two-way electrocatalytic activity upon both oxidation and reduction of uric acid. Similar to a bare glassy carbon electrode, uric acid undergoes a 2e,2H+ oxidation in phosphate buffer in the modified electrode. A diimine, the oxidation product of uric acid, was found to be an unstable intermediate, which was converted by a follow-up hydration reaction to an imine alcohol, with the reaction rate constant of 8.5 +/- 0.3 M(-1).s(-1) according to Nicholson's theory. Under optimum conditions, linear calibration graphs were obtained over the concentration range of 1.0 x 10(-7) M approximately 1.0 x 10(-5) M (uric acid) and 1.0 x 10(-5) M approximately 6.0 x 10(-4) M (adenine). Based on the signal-to-noise ratio of 3, the detection limits of the current technique was found to be as low as 9.0 x 10(-8) M (uric acid) and 2.0 x 10(-6) M (adenine), respectively. This novel biosensor was successfully applied for the assay of uric acid in human urine. Because of its good stability and long-term durability, such a gel modified electrode can provide a simple and easy approach for sensitive detection of uric acid and adenine.

Adenine↗
PubMed1987

Uric acid protects erythrocytes from ozone-induced changes.

Uric acid effectively reduced hemolysis and methemoglobin formation in bovine and swine erythrocytes bubbled with ozone in vitro. In bovine erythrocytes, formation of thiobarbituric acid-reactive material was inhibited by uric acid, but there was little immediate protection for the swine cells. Antioxidant protection was due to preferential degradation of the uric acid by ozone. These results provide evidence to support the hypothesis that in plasma, uric acid can provide antioxidant protection for erythrocytes.

Animals↗
PubMed1978

A solubility problem in the preparation of uric acid standards.

Consistently high (13-16%) uric acid values for quality control sera were found when using freshly-prepared working uric acid standards on the Autoanalyser II system. After investigation several conclusions are made, with the recommendation that working uric acid standards are best diluted with pH 9.5 glycine buffer (0.007 M).

Buffers↗
PubMed2001

Renal handling of uric acid assessed by means of pharmacological tests in obese women.

The aim of this study was to compare the renal handling of uric acid by means of pyrazinamide and probenecid tests between obese and non-obese women. A cross-sectional study was carried out in 8 obese women and in 8 non-obese women as control group. Metabolic profile and renal handling of uric acid including clearance, fractional excretion and excretion rates, were assessed. Due to technical problems, pyrazinamide and probenecid tests were performed only in 5 women of each group to evaluate presecretory reabsorption, secretion and post-secretory reabsorption of uric acid. Uric acid clearance had a tendency to be lower in the obese women than in the control group. There were no significant differences between the groups in fractional excretion and excretion uric acid rates. Pre- and post-secretory reabsorptions of uric acid did not differ between the obese and the non-obese women. Tubular secretion of uric acid was significantly lower in the obese women compared with the control group (6.4 vs 13.6%; p=0.02). Tubular secretion of uric acid negatively correlated with body mass index (r=-0.73; p<0.05). In conclusion, tubular secretion of uric acid possibly plays an important role in uric acid homeostasis in obese women.

Absorption↗
PubMed2002

Uric acid and urea in human sweat.

The present study investigated whether thermal sweating may relieve elevated concentrations of serum uric acid or urea. Concentrations of uric acid and urea were measured in the sweat of sixteen male volunteers, who were treated with external heat after one hour of intense physical exercise. The same analytes were also measured in their urine and serum samples. Furthermore, creatinine and some electrolytes were determined in these specimens. The results show that the concentration of uric acid in the sweat is 24.5 micromol/L, which is only 6.3% of that in serum. The concentration of urea in the sweat is 22.2 mmol/L, which is 3.6 times that in serum. The results indicate that sweat uric acid concentration is quite minimal, and the estimated total uric acid excretion per day in normal physiological range is insignificant. However, the level of sweat urea was found at a much higher concentration than the serum level. No correlation could be established between the level of uric acid in sweat and in serum. There was also no correlation between the level of urea in sweat and that in serum. These results suggest it would not be effective to relieve the elevated serum uric acid concentration by thermal sweating when the renal excretion of uric acid is partly compromised. Nevertheless, the potential of urea excretion via profuse sweating is apparent particularly when the kidneys are damaged or their function is impaired. These findings also suggest that persons who take vigorous exercise or are exposed to hot environments should be well advised to drink adequate fluids since heavy sweating excretes only minimal uric acid, accompanied by significant diminution of urinary output and diminished urinary excretions of uric acid, which may induce elevated levels of serum uric acid.

Adult↗
PubMed1975

Effect of paracetamol on uric acid determination.

The effect of paracetamol on uric acid determination using a phosphotungstate reduction method has been investigated. The results show that apparently raised values of serum uric acid may be reported in patients receiving therapeutic levels of this drug. Levels of serum uric acid were determined over a five-hour period in three patients who had received therapeutic doses of paracetamol. The assays of serum uric acid were performed by a method based on phosphotungstate reduction and by one employing uricase. The results illustrate the problems of using the former method for clinical purposes.

Acetaminophen↗
PubMed2006

Hormonal and cytokine effects of uric acid.

PURPOSE OF REVIEW: Current evidence supports the role of soluble uric acid as a true mediator of injury, exerting its effects through the induction of growth factors, cytokines, hormones and autacoids. In the present review, we summarize recent studies on the mechanisms involved in the uric acid deleterious effects. RECENT FINDINGS: Although uric acid is considered an antioxidant in plasma, recent clinical and epidemiological studies have found that hyperuricemia is associated with mortality and development of hypertension, cardiovascular and chronic renal diseases. Experimental studies suggest that uric acid induce its detrimental effects at the cellular level entering to vascular smooth muscle cells (VSMC) via an organic anion transport system, and followed by the activation of specific MAP kinases, nuclear transcription factors, with stimulation of COX-2, PDGF A and C chain, PDGF alpha receptor, and various inflammatory mediators, including C-reactive protein and monocyte chemoattractant protein-1. Physiologically, these effects translate into a rise of arterial pressure, VSMC hypertrophy, tubulointerstitial infiltration and glomerular hypertension in the setting of renal vasoconstriction. Uric acid also promotes endothelial dysfunction through inactivation of NO and arresting the proliferation of endothelial cells. Thus, arteriosclerosis induced by hyperuricemia may be a novel mechanism for the development of essential hypertension. SUMMARY: Soluble uric acid has important biologic roles. While it acts as an antioxidant, there is also evidence that uric acid has pro-inflammatory and proliferative effects on VSMC, and causes dysfunction of endothelial cells. These cellular mechanisms may translate into why uric acid is associated with renal and cardiovascular disease.

Antioxidants↗
PubMed1996

Abnormal serum uric acid levels in children.

Measurement of the serum uric acid level, most commonly considered in adult patients, is frequently obtained inadvertently for pediatric patients because it is a standard component of many multichannel chemistry profiles offered by clinical laboratories. Most standard references for normal uric acid values do not take into account the impact of the metabolic changes in children at different ages on the uric acid level. A substantial number of childhood conditions may produce perturbations in the serum uric acid level. Knowledge of normal serum uric acid levels and of the conditions affecting those levels in children enables a more focused pursuit of underlying abnormalities.

Adolescent↗
PubMed2003

Serum uric acid in hypertensive patients with and without peripheral arterial disease.

BACKGROUND: Uric acid is frequently elevated in hypertension. In addition to renal and metabolic disturbances, lower limb ischemia might contribute to hyperuricemia among hypertensives complicated by peripheral arterial disease (PAD). OBJECTIVE: To test the hypothesis that uric acid status is related to lower limb function in hypertensives with PAD. METHODS: Serum and 24-h urine uric acid levels and other risk factors were examined in 145 hypertensives free of PAD and 166 hypertensives with PAD. Ankle/brachial index (ABI) and absolute claudication distance (in PAD) on a treadmill test (ACD) were assessed. RESULTS: In multiple regression analysis for serum uric acid in the total group, PAD emerged as an independent determinant (P=0.03) next to age (P=0.005), triglycerides (P=0.04), and insulin (P=0.02). Serum uric acid concentrations were higher in hypertensives with PAD (404+/-101 vs. 347+/-80 micromol/l, P<0.001) independent of components of the metabolic syndrome (body mass index, triglycerides, insulin) and of age, gender, diabetes mellitus, pulse pressure, cholesterol, C-reactive protein, and treatment. After adjustment for kidney function by uric acid/creatinine ratio, values remained higher in hypertensives with PAD (P=0.01). Uric acid excretion was higher in the PAD group (P<0.001), whereas uric acid clearance was comparable between both groups. In multiple regression analysis for ACD (357+/-183 m) in the PAD group, serum uric acid (P=0.02), C-reactive protein (P<0.0001), age (P=0.02), and smoking (P=0.004) were independently associated. ABI (0.62+/-0.17) was not related to uric acid in PAD patients. CONCLUSION: Hyperuricemia is more pronounced in hypertensives complicated by PAD and is associated with worse functional status of the peripheral circulation.

Aged↗
PubMed2004

Uric acid administration for neuroprotection in patients with acute brain ischemia.

Uric acid is the end product of purine metabolism and a powerful water-soluble antioxidant and radical scavenger in humans whose generation is increased in situations of oxidative stress, such as brain ischemia. Although hyperuricemia has been related to an increased risk of cardiovascular events, the association was not found significant in many studies after adjustment for the effect of confounders. In the ischemic rat brain, the administration of uric acid results in neuroprotection and improved behavioral outcome. The severity of neurological impairment and the volume of infarction in patients with stroke have been found inversely related to the concentration of uric acid. In healthy volunteers, uric acid has been administered without untoward effects to show a conspicuous reduction of oxidative stress. We hypothesize that the administration of uric acid could be beneficial and cost effective in patients sustaining acute oxidative stress, such as those with acute ischemic stroke. Uric acid could also extend to more than 3 h the therapeutic window of rt-PA after stroke and it could limit the appearance of neurobehavioral changes after cardiopulmonary bypass. Prospective double blind randomized controlled trials are needed to test the value of uric acid in these clinical settings in which oxyradical formation is prominent.

Acute Disease↗
PubMed2003

[Oral chemolysis of uric acid stones].

Oral chemolysis of uric acid stones was performed retrospectively. Twenty-one patients with upper urinary uric acid stones were given alkaline citrate (Uralyt-U) orally. In the case of hyperuicemia, allopirinol was combined. In 11 out of 15 patients (73.3%) treated with oral chemolysis alone, stones were dissolved. In 4 out of 6 cases (66.7%) combined with extracorporeal shock-wave lithotripsy, administration of alkaline citrate shortened the period to be stone-free. In conclusion, we successfully treated 15 out of 21 cases (71.4%) with the administration of alkaline citrate.

Administration, Oral↗
PubMed2001

Comparative effects of losartan and irbesartan on serum uric acid in hypertensive patients with hyperuricaemia and gout.

OBJECTIVE: Losartan has been shown to increase urinary uric acid excretion and hence to lower serum uric acid levels. The purposes of the present study were: (1) to evaluate the effects of losartan on serum uric acid in hypertensive patients with hyperuricemia and gout, (2) to compare the effects of losartan with those of irbesartan, another angiotensin II receptor antagonist and (3) to evaluate whether losartan 50 mg b.i.d. has a greater impact on serum uric acid levels than losartan 50 mg once a day. METHODS: Thirteen hypertensive patients with hyperuricaemia and gout completed this prospective, randomized, double-blind, cross-over study. Uric acid-lowering drugs were stopped 3 weeks before the beginning of the study. Patients were randomized to receive either losartan 50 mg or irbesartan 150 mg once a day, for 4 weeks. During this phase, a placebo was given in the evening. After 4 weeks, the dose was increased to losartan 50 mg b.i.d., or irbesartan 150 mg b.i.d. for another 4 week period. Subsequently, the patients were switched to the alternative treatment modality. Enalapril (20 mg o.d.) was given during the run-in period and between the two treatment phases. Serum and urinary uric acid were measured at the beginning and at the end of each treatment phase. RESULTS: Our results show that losartan 50 mg once daily decreased serum uric acid levels from 538 +/- 26 to 491 +/- 20 micromol/l (P < 0.01). Irbesartan had no effect on serum uric acid. Increasing the dose of losartan from 50 mg o.d. to 50 mg twice a day, did not further decrease serum uric acid. This may in part be due to a low compliance to the evening dose as measured with an electronic device. Indeed, whatever the prescribed drug, the mean compliance of the evening dose was always significantly lower than that of the morning dose. The uricosuric effect of losartan appears to decrease with time when a new steady state of lower serum uric acid is reached. CONCLUSIONS: In contrast to irbesartan, losartan was uricosuric and decreased serum uric acid levels. Losartan 50 mg b.i.d. did not produce a greater fall in serum uric acid than losartan once a day. Losartan might be a useful therapeutic tool to control blood pressure and reduce serum uric acid levels in hypertensive patients with hyperuricaemia and gout.

Aged↗
PubMed1976

Renal excretion of uric acid during prolonged fasting.

Serum and urine uric acid were evaluated during prolonged therapeutic fasting in 15 obese patients. With increasing ketonemia the serum uric acid rose from a control value of 5.9 +/- 0.4 to 12.5 +/- 1.0 mg/100 ml at 7 days and then decreased progressively to 7.7 +/- 1.3 mg/100 ml by 28 days despite sustained ketonemia. The uric acid clearance were 5.5 +/- 0.9, 1.8 +/- 0.2, and 4.4 +/- 1.5 ml/min at days 0, 7, and 25 of fasting. At the same times the creatinine clearances were 114 +/- 11, 80 +/- 6, and 64 +/- 6.3 ml/min. There was no evidence of a renal tubular abnormality as assessed by glycosuria, bicarbonaturia, or increased phosphaturia. Urate binding to plasma proteins remained unchanged. Acute studies of the renal handling of uric acid revealed a uricosuric response to the administration of sodium lactate or sodium bicarbonate by intravenous infusion and low-dose acetylsalicylic acid orally. This renal tubular response departs significantly from that observed during the overnight fasted state and could not be accounted for by extracellular fluid volume expansion or the induced acid-base changes.

Adolescent↗
PubMed1995

Maternal serum uric acid levels in twin gestations.

OBJECTIVE: To establish normative values of serum uric acid levels in women with twin gestations and to compare maternal serum uric acid levels of twins and singletons, stratified by the presence or absence of preeclampsia. METHODS: Sixty-seven normotensive and 16 preeclamptic women with twin gestations, who had no underlying chronic hypertension or renal insufficiency, had serum uric acid levels measured on admission to the labor and delivery unit. These levels were compared with those of 83 normotensive and 10 preeclamptic singleton gravidas admitted to the same unit. A receiver operating characteristic (ROC) curve was used to determine the optimal maternal serum uric acid cutoff value for twin gestations and to compare this value with that of singleton gestations. RESULTS: Women with non-preeclamptic twin pregnancies had significantly higher mean (+/- standard deviation) serum uric acid concentration than women with non-preeclamptic singleton pregnancies (5.4 +/- 1.6 versus 4.7 +/- 1.2 mg/dL, respectively, P = .001). Gravidas with twin gestations complicated by preeclampsia had significantly higher serum uric acid levels than their preeclamptic singleton counterparts (7.7 +/- 1.3 versus 5.9 +/- 1.1 mg/dL, respectively, P = .001). Using a ROC curve, we determined that a maternal serum uric acid level of 6.5 mg/dL appeared to be the optimal cutoff for identifying preeclampsia in twin gestations, with a sensitivity of 94% and specificity of 78%. CONCLUSION: With or without preeclampsia, women carrying twins have significantly higher serum uric acid levels than their singleton counterparts, which suggests a need for separate normative values for twin gestations. We propose that a serum uric acid level of 6.5 mg/dL or greater be used to identify those women with twin gestations who are at higher risk for preeclampsia.

Adolescent↗
PubMed1986

Uric acid and phosphorus excretion in dogs with lymphosarcoma.

Serum uric acid and phosphorus concentrations were determined for 27 dogs with multicentric lymphosarcoma before and after chemotherapy. Mean serum uric acid values in dogs before treatment were significantly higher (P less than 0.05) than those of a control group of healthy dogs. Serum uric acid values did not change after treatment. Of the 27 dogs, 13 had 24-hour urine collections to determine endogenous creatinine clearance and quantitation of uric acid and phosphorus excretion before and after treatment for lymphosarcoma. Mean values for 24-hour creatinine clearance before and after treatment were statistically similar in dogs with lymphosarcoma, although the values were lower than those in a normal range. Total urinary phosphorus excretions were increased significantly (P less than 0.01) after treatment without change in fractional excretion. Chemotherapeutic agents used accounted for the significant (P less than 0.05) increase in urine volume after treatment and may have affected the excretion of uric acid and phosphorus. Seemingly, dogs with uncomplicated lymphosarcoma rarely have renal dysfunction or clinically important alterations in uric acid or phosphorus excretion secondary to rapid tumor lysis. However, preexisting renal disease or systemic complications, such as hypercalcemia, may be associated with increased risk of further renal impairment during treatment.

Animals↗